Abstract

BackgroundBulimia Nervosa (BN) is believed to be caused by an interaction of genetic and environmental factors. Previous studies support the existence of a bulimia-related endophenotype as well as disturbances in serotonin (5-HT) transmission. We studied serotonin transporter (SERT) binding in BN, and to investigate the possibility of a SERT-related endophenotype for BN, did this in a sample of female twins. We hypothesized clearly reduced SERT binding in BN women as opposed to healthy women, and intermediate SERT binding in unaffected co-twins.MethodsWe studied 13 female twins with BN (9 with purging and 4 with non-purging BN) and 25 healthy women, including 6 healthy twin sisters of BN patients and 19 women from 10 healthy twin pairs. [123I]ADAM, a selective SERT radioligand for single photon emission tomography (SPET) imaging, was used to assess SERT availability in the midbrain and the thalamus.ResultsNo differences in SERT binding were evident when comparing the BN women, their unaffected co-twins and the healthy controls (p = 0.14). The healthy sisters of the BN patients and the healthy control women had similar SERT binding in both brain regions. In a post hoc subgroup analysis, the purging bulimics had higher SERT binding than the healthy women in the midbrain (p = 0.03), but not in the thalamus.ConclusionOur finding of increased SERT binding in the midbrain in the purging BN women raises the possibility that this subgroup of bulimics might differ in serotonergic function from the non-purging ones. The similarity of the unaffected co-twins and the healthy controls doesn't support our initial assumption of a SERT-related endophenotype for BN. Due to the small sample size, our results need to be interpreted with caution and verified in a larger sample.

Highlights

  • Bulimia Nervosa (BN) is believed to be caused by an interaction of genetic and environmental factors

  • The aim of this study was to (1) investigate whether the finding of reduced serotonin transporter (SERT) binding in subjects with BN observed using the less selective radioligand [123I]β-CIT [18] can be replicated with [123I]ADAM, and (2) to explore the possible genetic background of BN by comparing [123I]ADAM binding to SERTs between subjects with BN, their healthy co-twins and healthy controls

  • Demographic variables and behavioral assessments The mean body mass indices (BMIs) and ages were similar for the 13 women with BN, their twin sisters and the healthy control twins (Table 1.) The mean age of onset of bulimia was 18.3 y (SD: 2.9 y, range: 13 – 21 y) and its mean duration was 6.5 y (SD: 4.4 y, range: 6 months – 14 y)

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Summary

Introduction

Bulimia Nervosa (BN) is believed to be caused by an interaction of genetic and environmental factors. Previous studies support the existence of a bulimia-related endophenotype as well as disturbances in serotonin (5-HT) transmission. We studied serotonin transporter (SERT) binding in BN, and to investigate the possibility of a SERT-related endophenotype for BN, did this in a sample of female twins. Subjects with symptomatic BN show several abnormalities in 5-HT metabolism and function [4,5,6,7,8,9]. Both women with current BN and women who have recovered from BN seem more vulnerable than healthy control women to the mood lowering and the binge precipitating effects of acute tryptophan depletion [10,11]. A wide range of antidepressant medications are effective in reducing binge and purge frequency [12,13]

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